Salles B, Weisemann J M, Weinstock G M
Department of Biochemistry and Molecular Biology, University of Texas Medical School, Houston 77057.
J Bacteriol. 1987 Nov;169(11):5028-34. doi: 10.1128/jb.169.11.5028-5034.1987.
The expression of the gene encoding colicin E1, cea, was studied in Escherichia coli by using cea-lacZ gene fusions. Expression of the fusions showed the same characteristics as those of the wild-type cea gene: induction by treatments that damage DNA and regulation by the SOS response, sensitivity to catabolite repression, and a low basal level of expression, despite the presence of the fusion in a multicopy plasmid. Induction of expression by DNA-damaging treatments was found to differ from other genes involved in the SOS response (exemplified by recA), in that higher levels of DNA damage were required and expression occurred only after a pronounced delay. The delay in expression following an inducing treatment was more pronounced under conditions of catabolite repression, indicating that the cyclic AMP-cyclic AMP receptor protein complex may play a role in induction. These observations also suggest a biological rationale for the control of cea expression by the SOS response and the cyclic AMP-cyclic AMP receptor protein catabolite repression system.
利用cea - lacZ基因融合技术，在大肠杆菌中研究了编码大肠杆菌素E1的基因cea的表达情况。融合基因的表达表现出与野生型cea基因相同的特征：受损伤DNA的处理诱导，受SOS反应调控，对分解代谢物阻遏敏感，且表达的基础水平较低，尽管融合基因存在于多拷贝质粒中。发现DNA损伤处理诱导的表达与其他参与SOS反应的基因（以recA为例）不同，即需要更高水平的DNA损伤，且表达仅在明显延迟后才发生。在分解代谢物阻遏条件下，诱导处理后表达的延迟更为明显，这表明环腺苷酸 - 环腺苷酸受体蛋白复合物可能在诱导过程中起作用。这些观察结果还为通过SOS反应和环腺苷酸 - 环腺苷酸受体蛋白分解代谢物阻遏系统控制cea表达提供了生物学依据。
